Increasing skeletal muscle growth after an induction of an atrophying inducing stimulus (i.e. disuse) is extremely important in various medical conditions. Skeletal muscle wasting can contribute to increased health care costs and a decreased quality of life. The proposed research would examine the mechanism that allows Leukemia Inhibitory Factor (LIF) to inducer satellite cell proliferation and the role it may play in muscle re- growth after 10 days of immobilization. This research would be novel in that it would identify a possible signaling mechanism that may regulate satellite cell proliferation and ultimately affect skeletal muscle growth. Further, the research would extend the role of a cytokine known to cause cardiac hypertrophy to skeletal muscle. This would be a completely novel finding. Pilot data that I have colleted indicates that LIF can induce myoblast proliferation, possibly by activating the NAK2-STAT2 or PI3K pathways. Also, I found that skeletal muscle expressed the LIF protein after 6 days of ambulatory recovery from 10 days of hindlimb immobilization. Therefore, it is proposed to determine which signaling cascades are necessary for LIF-indued satellite proliferation and to determine if this pathway extends to the whole animal. Identification of a cytokine and a signaling mechanism that may regulate muscle growth could lead to other counter-measures to ultimately prevent muscle wasting.